Nuevas proyecciones fisiológicas, patológicas y terapéuticas de la leptina / Novel physiological and therapeutic implications of leptin

The adipose tissue is an endocrine organ that produces a variety of protein hormones. One of them is leptin, which regulates several critical functions at the central nervous system such as caloric intake, basal energy expenditure, reproduction, glucose and lipid metabolism and osteogenesis. Acting at a local level, leptin modulates the immune system and promotes liver fibrogenesis. The most promising therapeutic implications of leptin will possibly be in type 1 diabetes mellitus (DM1). Its supplementation in animal models of DM1 prevents hyperglycemia and ketoacidosis. These actions depend on the activation of leptin receptors in the central nervous system and the suppression of glucagon signaling in the liver.

La hipótesis de Pedersen no es suficiente: Otros nutrientes además de la glucosaexplicarían la macrosomía fetal enpacientes diabéticas gestacionales consobrepeso y buen control glicémico / Nutrients other than glucose might explain fetal overgrowth in gestationaldiabetic pregnancies

Since 1964, the hypothesis of Pedersen has been used to explain fetal macrosomia observed in gestational diabetes mellitus (GDM), by a mechanism involving maternal hyperglycemia - fetal hyperglycemia - fetal hyperinsulinemia. However,since the 1980-89 decade, it is known that pregnant women with pre-gestationaloverweight not suffering from GDM still have a higher frequency of fetal macrosomia. Furthermore, pregnant women with GDM, despite being subjected to optimalglycemic control, still show unacceptably high frequencies of fetal macrosomia, aphenomenon that is concentrated in pregnancies with overweight or obesity priorto pregnancy. If glucose is not the single nutrient responsible for fetal macrosomiain pregnant women with gestational diabetes that undergo strict glycemic control,other nutrients may cause excessive fetal growth in pre-pregnancy overweightmothers. In this review, we propose that triglycerides (TG) could be responsible forthis accelerated fetal growth. If this hypothesis is validated in animal models andclinical studies, then normal and pathological ranges of TG should be defined, andmonitoring of triglyceride levels during pregnancy should be advised as a possiblenew alternative, besides a good glycemic control, for the management of fetal macrosomia in GDM women with overweight prior to pregnancy.